Molecular basis for tumor progression triggered by genetic heterogeneity of oncogenic activities.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25640064
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Kyoto University
• Principal Investigator: IGAKI Tatsushi 京都大学, 生命科学研究科, 教授 (00467648)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: がん / 細胞間相互作用 / 遺伝的不均質性 / ショウジョウバエ / Ras / Src

Outline of Final Research Achievements

During cancer progression, clones of cells with different oncogenic mutations can interact with each other, leading to the promotion of cell proliferation and metastatic ability. To understand the molecular mechanisms of cancer progression triggered by the heterogeneity of cells with different oncogenic activities, we used a new Drosophila genetic mosaic technique called ‘coupled-MARCM’ technique. Through a genetic screen and subsequent genetic analyses, we found that a heterogeneity of cell clones with elevated Ras or Src oncoprotein activity triggers tumor progression in Drosophila imaginal epithelium. Furthermore, we elucidated the Notch-Delta-based mechanism of this tumor progression triggered by the interaction between Ras- and Src-activated cell clones.

Free Research Field

発生遺伝学、腫瘍学